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Both diseases share hippocampal atrophy, hypoperfusion, hypometabolism, mitochondrial dysfunction, slowed cerebral bloodflow, hypoxia and neurodegeneration--which are known to affect gait and cognition.According to Dr. Peter Stys, Alheimer's and MS share many things in common, but inflammation has thrown researchers off track. Indeed, age of onset may be the major difference between the two diseases.

Because diseases such as Alzheimer’s and Parkinson’s have a much more prominentdegenerative rather than inflammatory phenotype, the initial assumption was that a degenerativemechanism (or mechanisms) was primarily responsible, with inflammation perhaps a secondary,but possibly important, consequence of the degeneration. In MS, the situation is reversed:inflammation occurs early and is very prominent in many patients, so it was naturally assumed thatautoimmunity might be causal; but, as we argue throughout this Perspective, such an assumptionmay be incorrect. If MS is primarily a degenerative disorder in line with an inside-out mechanism,why would this disease be unique in engendering such prominent and cyclic inflammation?

The differences may be related to age: Alzheimer’s disease and Parkinson’s disease present decadeslater than MS, and immune responsiveness wanes with age through a process of ‘immunesenescence’ (REFS 21,87). Indeed, the responsiveness of T cells, which are known to be centrallyinvolved in the immunopathogenesis of MS88, appears to be particularly altered with age87.Moreover, it is conceivable that the putative cytodegeneration involving the myelinating unit(oligodendroglia, their processes and myelin) in MS releases debris that is more antigenic35,36,66 thanthe debris that is shed from the mainly synaptic and neuronal degeneration in Alzheimer’s disease.

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